Evidence map›Paper›PMID 36576166›Full record

ReviewCell cycle (Georgetown, Tex.)2023

The role of cyclin Y in normal and pathological cells.

Aleksandra Opacka, Agnieszka Żuryń, Adrian Krajewski, Klaudia Mikołajczyk

Open access · greenAbstract readReview
In one paragraph

Review in Cell cycle (Georgetown, Tex.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 32% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Aleksandra OpackaDepartment of Histology and Embryology, Nicolaus Copernicus University in Toruń, Bydgoszcz, Poland.
Agnieszka ŻuryńDepartment of Histology and Embryology, Nicolaus Copernicus University in Toruń, Bydgoszcz, Poland.
Adrian KrajewskiDepartment of Histology and Embryology, Nicolaus Copernicus University in Toruń, Bydgoszcz, Poland.ORCID 0000-0001-9172-2698
Klaudia MikołajczykDepartment of Histology and Embryology, Nicolaus Copernicus University in Toruń, Bydgoszcz, Poland.
Nicolaus Copernicus University · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The family protein of cyclins, as well as cyclin-dependent kinases (CDKs) cooperating with them, are broadly researched, as a matter of their dysfunction may lead to tumor transformation. Cyclins are defined as key regulators that have a controlling function of the mammalian nuclear cell divides. Cyclin Y (CCNY) is a recently characterized member of the cyclin family and was first identified from the human testis cDNA library. It is an actin-binding protein acting through decreased actin dynamics at a steady state and during glycine-induced long-term potentiation (LTP) and involves the inhibition of cofilin activation. What is more, CCNY is a positive regulatory subunit of the CDK14/PFTK1 complexes affected by the activation of the Wnt signaling pathway in the G2/M phase by recruiting CDK14/PFTK1 to the plasma membrane and promoting phosphorylation of LRP6. The expression of CCNY has been significantly mentioned within the cell migration and invasion activity both in vivo and in vitro. The aim of this review is evaluation of the expression of CCNY in the physiology processes and compare the expression of this protein in cancer cells, taking into account the impact of the level of expression on tumor progression.

Indexed as

Cyclin-Dependent KinasesTestisAnimalsCell NucleusCyclinsHumansMaleMammalsPhosphorylationCCNY protein, humanCDK14 protein, humanCyclin-Dependent KinasesCyclinsautophagycancercell cyclecyclin Yneural developmentWnt signalling

Identifiers

PMID36576166
PMCPMC10054165
OpenAlexW4313236976

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.